As I read the daily news in the field of brain health, I see the same facts used to support and round out almost every article on Alzheimer's disease. There is nearly always a reference to the 5.5 million Americans stricken, usually a brief description of the disease as a "progressive neurological disorder", and frequently, the nihilistic proclamation that there is no cure.

It is true of course; there is no cure. However, I am alarmed by the tendency of many to interpret that to mean that there is no treatment, which is inaccurate. The two statements are very different.

This problem doesn't seem to plague other diseases. There is no cure for hypertension or diabetes but that particular comment never seems to be appended to related news stories. Ditto for high cholesterol and osteoporosis. With all of those maladies, and many others, we have grown entirely comfortable with the notion of identifying them and treating them to best manage their forward course.

The reality is that Alzheimer's disease can be treated. Not yet with the efficacy with which we treat other diseases like those I mentioned but certainly well enough that people with memory concerns should pursue a diagnosis and, if it is Alzheimer's disease, seek treatment.

There is no denying that we need better treatments and ultimately a cure. In the meantime, a good diet, physical exercise, social engagement, and poly-therapy including a cholinesterase inhibitor plus Namenda can have a meaningful impact on the disease within many patients. We have no cure but that does not mean we have no treatment.

As we write here often, education and awareness about Alzheimer's disease will help to reduce the stigma of memory loss and promote more timely intervention. Please share this information with your online networks using the share button below.

According to a study from the French National Institute for Health and Medical Research, it appears as though Alzheimer's patients with diabetes lose memory function more slowly than Alzheimer's patients without diabetes. This seems counter-intuitive given that diabetes increases the risk for both Alzheimer's and for memory loss.

In fact, this study published in the October 27, 2009 issues of Neurology, may not be as conclusive as it seems on the surface. The study followed 608 Alzheimer's patients, about ten percent of whom also had diabetes, and assessed their memory twice annually for the four year duration of the study. The results showed that the diabetes group fell about four tenths of a point on a 20-point cognitive scale every six months whereas the group with no diabetes fell about three times as much; about one and a quarter points at each interval.

However, a few limitations in the study prevent a tidy conclusion. Most glaringly, the cognition of those in the diabetes group may have benefited from the diabetes treatments they took in addition to the Alzheimer's treatments. It was also unclear if the diabetes group and the no-diabetes group had similar levels of cognition at the start of the study. If the diabetes group was more impaired (that is, had already declined more precipitously), then a slower ongoing descent would be considerably less interesting.

One of the keys to better Alzheimer's care is education. We need a more informed public that knows how and when to seek expert advice from a medical doctor. We also need the medical community to adopt a consistent approach to applying the latest standards of care for an aging public with many memory concerns, be they real concerns or false alarms.

While there is a lot of information posted online that can help educate the public, there is also lots of suspect information as well. One site that has a wealth of high quality information in this field is www.caring.com. You may have noticed one of their articles that was picked up by the general media; it described the types of information a family will want to collect and consider if they suspect the early stages of Alzheimer's disease.

The article outlines six practical steps to take when memory concerns are first present. Following these steps should keep the diagnostic process moving in a constructive direction toward a beneficial conclusion. The steps, each examined in more detail in the full article, include:

Creating a record - writing down observations about the nature and frequency of any behaviors that seem problematic.

Educating yourself - learning about all the possible explanations for cognitive changes to avoid jumping to an overly dire conclusion.

Identifying a qualified physician - this may be the patient's usual primary care physician but it may not be. Not all M.D.'s are equal.

Getting a thorough diagnostic work-up - this will include more than a medical history and a physical exam as blood work, cognitive assessment, and brain imaging may all be required.

Seeing a specialist - whether the primary care physician initiates this step or not, the family should pursue such a consultation.

Seeking a second opinion - as the medical community endeavors to absorb new medical knowledge in this field, there is a wide range of expertise among primary care physicians. Getting a second opinion is a prudent step.

We write about this topic frequently as the general media tend to be fairly inconsistent in their characterization of dementia. As we are careful to point out, dementia is the loss of cognitive capacity that results from various diseases, accidents, and medical conditions. In and of itself, dementia is not a disease.

Having said that, an important new perspective presented this month by Time might add ongoing confusion to this topic. In a well-written piece, based on a publication in the New England Journal of Medicine, researchers advocate the perspective that patients actually die of dementia. This perspective is akin to viewing dementia as a disease, not a symptom of other medical problems.

While I agree with the author's main point, that patients with dementia are suffering all sorts of systemic biological failures due to a progressive level of brain damage (and will most likely die from these failures), it is the underlying diseases that produce both the dementia and the death.

One key point in the article that I want to support and emphasize is this: For physicians and caregivers, it is important to recognize that, once demented, the patient's health may have reached such a poor state that a focus on palliative care is warranted over aggressive treatment of the underlying problems. While I think it would create undue confusion to define "dementia" as a disease and to identify it as a "cause of death", the point about approaches to better care is well taken and should be noted.

There is no definitive answer to this ubiquitous question. The best we can do is to watch the advance of science through the published literature and to follow the clinical trials from which the answer will one day emerge.

While the pathology of Alzheimer's disease is still not well understood, scientists have developed a host of well-grounded theories. Several treatment agents, based on those theoretical foundations, are currently in development or in clinical trial. Here is a short summary of the three leading treatment hypotheses:

The Cholinergic hypothesis proposes that AD is caused by reduced function of a certain chemical in the brain called acetylcholine. The chemical is known to be important in memory formation and brains of patients with AD have less acetylcholine. In fact, most medications currently approved for AD act by increasing acetylcholine levels in the brain. However, their ability to treat the disease has been limited, indicating other factors at play.

The Amyoid Hypothesis states that a buildup of deposits (amyloid) is the fundamental cause of Alzheimer’s disease. It is a compelling theory because a gene associated with this form of amyloid is located on chromosome 21 and people with an extra copy of this gene (those with Down Syndrome) almost universally exhibit AD by 40 years of age. Also, APOE4, the major genetic risk factor for AD, leads to excess amyloid buildup in the brain before AD symptoms arise. Thus, amyloid buildup precedes clinical AD.

The Tau Hypothesis encompasses the idea that tau protein abnormalities form damaging tangles inside nerve cells. When this occurs, the cell's transport systems disintegrate and malfunction which may disrupt communications between cells and later cause cell death.

While these are the primary theoretical drivers of drug development, there are other agents in clinical trial that were not developed on the basis of a particular theoretical approach to the disease. Dimebon, currently in Phase III FDA trial is a pre-approved antihistamine that was shown to correlate with low dementia prevalence. Although scientists are not sure how or why it might effectively treat Alzheimer’s disease, results of the Phase I and II trials were positive and Dimebon may in fact be the next approved treatment for Alzheimer’s disease.

While it is premature to say that a cure is imminent, it should be clear that several treatment agents are in advanced stages of clinical trial. However, predicting the results of these trials is hampered by our vague understanding of what causes Alzheimer's Disease. On the bright side, one or another of these agents may be surprisingly effective in altering the disease course and could be available in two to five years. On the dark side, they may all turn out to be ineffective in which case we would be more than five years away from a meaningful new medication. Only time will tell.

In the meantime, we all need to be proactive in identifying and managing our risk factors for cognitive decline and physicians must be vigilant about acting on evidence or suspicion of decline among their patients. Until better treatments are discovered, we must intervene as early as possible with the current medications to maximally delay the progression of Alzheimer's disease.

Remember, we need a cure but there is much we can do while we await its arrival. Current treatments are more effective than many headlines suggest. With early intervention and a robust therapeutic regimen (including physical exercise, mental and social activity, a healthy diet, and currently approved medications), we can already meaningfully delay the progression of this terrible disease.

Bio-marker development is a very common news topic in the Alzheimer's field. Each day there is news about a blood test, a spinal assay, a binding agent that aids imaging, or a new cognitive measure. These developments are important as they will lead the way to earlier detection and more accurate diagnoses -- two areas where improvements could have a great positive impact on treatment outcomes.

A particular approach that has gotten a lot of media attention, including this story today, is to measure the amount of beta-amyloid in the blood. The theory is that people with subtle memory loss and high levels of beta-amyloid may be in the early stages of Alzheimer's disease and should be treated immediately before symptoms worsen. Those with subtle memory loss and normal levels of beta-amyloid probably have some other medical condition disturbing their memory.

While this work is theoretically intriguing, one particular obstacle still stands in the way of clinical utility. The challenge is that the beta-amyloid levels in the blood of healthy individuals range widely. Therefore, it is difficult to meaningfully identify the "normal" level in any given patient. As such, measuring amyloid in the blood or spinal fluid is a promising avenue but still quite some time from clinical feasibility.

One possible improvement in this approach is to compare the ratio of beta-amyloid to tau proteins in the blood. Doing so may offer a more meaningful measure, particularly when observed over time within a given patient. A rapidly changing ratio may indicate pathological changes that foretell the onset of Alzheimer's disease. Work on this approach is proceeding at several locations.

We look forward to ongoing news and developments in this area. For the time being, the most accurate and clinically feasible bio-marker is cognition. Eventually, it is likely that a combination of biomarkers will be used in conjunction to accurately identify diseases and medical conditions in early stages when treatment effect is optimal.

If you read many of the recent headlines you might think so. A closer look at the study producing those headlines suggests that some of them are probably worded a bit more strongly than the research can support.

The good news is that this study provides further confirmation that ongoing intellectual stimulation is usually correlated with lower prevalence of dementia. We have seen this in many studies and there can be little doubt that using your brain creatively, to solve problems, to socialize, and to learn new information or skills is generally beneficial to cognitive health.

An important message that is sometimes lost amid the rush to identify those games and activities that provide the most effective work-out for the brain, is that many simpler and more natural human activities also provide a healthy cognitive challenge. One activity that requires a broad range of cognitive skills is making and maintaining personal relationships.

The key take away is this: Don't underestimate the importance of social activity as you seek new ways to exercise your brain. Perhaps joining a club or volunteering could bring you a natural and rewarding approach to the sought after cognitive benefits.

You may have seen this story elsewhere in the news but it bears repeating here as we view diet to be one of the most well studied and most effective approaches to maintaining good cognitive health. Our food intake is one of the factors that is most easily within our control and appears to have an important impact on risk for Alzheimer's disease.

According to a study at Columbia University and presented at the annual meeting of the American Neurological Association, a diet rich in cruciferous and green leafy vegetables, nuts, fish, and tomatoes and low in red meat and high-fat dairy products may be protective against Alzheimer's disease.

In the study, 1,691 subjects aged 65 and older with no signs of cognitive impairment were surveyed about their dietary habits. Based on the amounts of protective nutrients (omega-3 fatty acids and vitamin E) and risk-increasing nutrients (saturated fatty acids) in each food, the researchers divided the subjects into groups. The groups were subsequently followed for 4 years to assess the rates at which each group showed cognitive decline.

The results showed that the 1/3 of subjects who most closely adhered to the "protective" diet was 38% less likely to be diagnosed with Alzheimer's disease in this time frame than the 1/3 of subjects who most deviated from that diet. These results held true even when age, physical activity, smoking, body mass index, and overall caloric intake were all controlled.

A 38% reduction in risk simply by eating well -- that's too good to pass up. We can't say it enough - eat your fruits and vegetables and cut back on some of the saturated fats.

Contributed by: Michael Rafii, M.D., Ph.D - Director of the Memory Disorders Clinic at the University of California, San Diego. ______________________________________

The layering of neurons in the developing brain requires Reelin, a protein located on the outside of the cells. Reelin, also acts as a "green light", stimulating neurons to respond more strongly to their neighbors' signals. A recent study showed that applying Reelin directly to brain slices from mice prevents excess beta-amyloid from completely silencing nerves. In the study conducted using mouse models, the researchers determined that Reelin and beta-amyloid interact with the same receptor, (the NMDA receptor), which plays an important role in coordinating chemical signals between adjacent neurons.

They found that Reelin activates and strengthens the response of the NMDA receptor. In the presence of too much beta-amyloid, the receptor goes back into the cell, reducing the cell's sensitivity to incoming signals. By contrast, in strong concentrations of Reelin, the receptor remains active and the cell has the "green light" to continue receiving normally.

More work will be needed to see if Reelin can be used as a potential treatment in AD.

Contributed by: Michael Rafii, M.D., Ph.D - Director of the Memory Disorders Clinic at the University of California, San Diego. ______________________________________

Former professional football players suffer from Alzheimer's disease or other memory-related conditions at rates far higher than the general population, a new study commissioned by the National Football League shows. Retired players between the ages of 30 and 49 are 19 times more likely to struggle with memory problems than similarly aged men who never played professional football, the study found. The findings could have implications that reach far beyond the National Football League. Head injuries are not uncommon among college and high school players.

The new study of former pro players has not been peer-reviewed, but the results mirror several other recent studies suggesting a link between dementia and head injuries. The results of the study, conducted by the University of Michigan's Institute for Social Research, were first reported by The New York Times this past September.

For the NFL survey, the Michigan researchers contacted 1,063 retired players by phone late last year. The players, who had to have played at least three seasons to qualify for the survey, were asked a series of questions on a series of topics, including questions on health, financial well-being and satisfaction with life. Most of the questions came from the standard National Health Interview Survey. That way, answers could be compared to previously collected data from the general population. In some cases, a player's wife answered the questions. The Michigan researchers found that, among players aged 50 and older, 6.1% of them said they had received a dementia-related diagnosis -- five times higher than the national average of 1.2%. Players between the ages of 30 and 49 had a dementia-related diagnosis rate of 1.9% -- 19 times higher than the national average of 0.1%, according to the survey.

The management of concussions has been a major area of research in the field of neurology the last few years, with the American Academy of Neurology having published guidelines on its management in the past year. Much more work is needed to identify the mechanism by which the concussion brings about the changes seen in AD, and where intervention is needed.

In the October 13 issue of Neurology, the American Academy of Neurology has published new treatment guidelines for amyotrophic lateral sclerosis (ALS), often called Lou Gehrig's disease.

The guidelines are designed to help physicians optimize the quality of life for their ALS patients. While many with ALS with succumb to the disease within 3 to 5 years, others live as long as ten years after diagnosis. For these patients in particular, much can be done to ensure overal health and comfort throughout the disease course.

A more complete summary and link to the full publication can be viewed here but the basic guidelines are as follows:

prescribe Riluzole, the only FDA approved drug for ALS

use an assisted-breathing device

use a feeding (PEG) tube

offer botulinum toxin B to treat drooling if oral medications do not help

enroll early in a specialized multidisciplinary ALS clinic to optimize care

As with other neurological disorders such as Parkinson's and Alzheimer's disease, there is no cure for ALS. However, as we see across all of these diseases, we have increased our ability to manage symptoms, prolong survival, and maintain a high quality of life. One key to such success is ongoing dissemination of guidelines outlining the highest standards of care.

According to a study published this month in Archives of Neurology, declining visuospatial skills may be one of the earliest cognitive indicators of emerging Alzheimer's disease. If confirmed, this could alter the current perspective that short-term memory is the earliest cognitive realm to show impairment.

In the study, conducted at the University of Kansas, 444 dementia-free subjects were enrolled and followed with a battery of neuropsychological assessments for an average of 5.9 years. During the course of the study, 134 subjects became demented and the cause of dementia was confirmed as Alzheimer's disease in 44 of them.

By looking at the performance of each subject across the battery of assessments, researchers were able to identify which realms of cognition declined earliest in those subjects who eventually suffered from dementia. The results suggested that multiple domains, including attention, executive function, episodic memory, and surprisingly, visuospatial skills may all play roles in indicating early stage cognitive decline.

This finding may shift the current emphasis from episodic memory to a broader set of domains, including visuospatial skills, in the ongoing effort to develop better assessments for detecting the onset of dementing disorders such as Alzheimer's disease.

I borrowed this headline directly from this article in today's Baltimore Sun.

The headline filled me with optimism that the article could be useful in my ongoing campaign to clarify the fact that "dementia" is not a disease but rather a symptom caused by many distinct medical conditions. I think it is important for all to understand that we don't "treat" dementia, rather, we treat the Alzheimer's or Parkinson's or stroke or other underlying cause of the dementia.

The headline makes it clear that dementia has more than one cause so I was hopeful that the body of the article would be beneficial in clarifying what I have summarized above. Alas, this is not the case and the article will be just one more of the many that add to the confusion around the term dementia.

However, the descriptions of the various causes of dementia are useful and accurate as are the summaries of typical symptoms associated with each cause of dementia. In this regard, the article is a worthy read. Just be sure to disregard the opening sentence stating that "Dementia is an illness..." because it is actually a symptom of some other problem.

According to a recent publication in Neurology, about one in eight strokes is preceded by a transient ischemic attack, known as a TIA, which is very mild stroke that usually produces only subtle and short lasting symptoms. The research suggests that noting and reacting to this warning can reduce the likelihood of a more serious stroke later.

Th importance of this study is highlighted by the fact that up to 80% of strokes that follow a TIA might be preventable with intensive management of risk factors. Risk factors that should be managed include hypertension, high cholesterol, smoking, diabetes, and obesity. Also important is expert evaluation (and intervention if necessary) following any symptoms of stroke, even mild symptoms from a TIA.

Please consider sharing this short posting (share button below) with any of your contacts who may be at risk for stroke.

There has been lots of news lately about concussion and its lingering effects on brain health. In fact, the recent publication of results from a study of NFL players (summarized here) has brought heightened awareness to the long-term risks associated with brain injury.

The LA Times recently published this excellent descriptive overview of what happens to the brain when it is concussed including an explanation of particular symptoms and why they may or may not linger. An important take-away is that the brain does have some ability to heal after an injury. For this reason, it is especially important to create an optimal healing environment following a concussion. This obviously includes protection against further head trauma but also includes ensuring a plentiful supply of oxygen rich blood and proper nutrition during the healing process.

These lesser known facts should be shared broadly to improve general understanding of how best to keep the brain healthy over the course of a long life.

Today at IrishTimes.com there is an excellent summary of the many influences on memory as we age. We have also commented here in the past about perceived types of memory decline that are very consistent with a normal and healthy advance in age.

In this time when there is so much angst over Alzheimer's disease, it is important to be informed and to keep a proper perspective about suspected decline in one's ability to store and retrieve information. Some types of memory disturbances indicate a potential problem and should be evaluated by a physician in a timely manner. Others are not really memory problems but are more the result of poor hearing, slow processing, or intermittent attention.

As always, we encourage you all to educate yourself about these matters and to see a physician immediately if you suspect an emerging problem with your memory.

In addition to distilling the daily news about brain health, this blog strives to promote a better understanding of terms and concepts relative to this topic. One term that is in the news every day but is commonly misused is "dementia". To help the readership gain a clear understanding, we have defined it here in a prior post.

The key point I always stress is that dementia is not a disease but a symptom of some underlying problem. Many diseases and medical conditions (Alzheimer's, stroke, trauma, thyroid deficiency, etc.) can lead to cognitive impairment (a symptom) which, if severe enough, will be classified as dementia.

Today there is a good piece in the South Bend Tribune that offers additional clarity and I encourage you all to click through and read it.